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Hesa-A Down-Regulates erb/b2 Oncogene Expression and Improves Outcome of Oral Carcinoma in a Rat Model
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 Title & Authors
Hesa-A Down-Regulates erb/b2 Oncogene Expression and Improves Outcome of Oral Carcinoma in a Rat Model
Abbasi, Mehran Mesgari; Mehdipour, Masoumeh; Monfaredan, Amir; Jahanban-Esfahlan, Rana;
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 Abstract
Background: Oral carcinoma (OC) remains one of the most difficult malignancies to cure. Hesa-A is an Iranian herbal-marine compound that has shown promising anti-tumor properties against various human tumors. However, its mechanism of action remains to be addressed. The present study was conducted to evaluate the effect of two doses of Hesa-A on mRNA expression of erbb2 as a main prognosticator tumor marker for OC in an animal model. Materials and Methods: A total of 60 rats were randomly divided into 5 groups of 12 animals each. Rats in carcinoma groups received 0, 250 and 500mg/kg body weight doses of Hesa-A 3 times a day. The other two groups were considered as treated and untreated control groups. At the end of the experiment, animals were sacrificed and tongue tissues subjected to H and E staining and real time PCR. Results: Our results showed that compared to the control group, erbb2 was over-expressed ~ 30% in the carcinoma group. After treatment with 250mg/kg and 500mg/kg body weight of Hesa-A, erbb2 levels dropped by 24.1% and 3.4 % respectively compared to the control carcinoma group (p<0.01, p<0.0001). Moreover, there was a significant relation between erbb2 mRNA content and observed pathological changes in studied groups (p<0.05). Conclusions: These data provide insight into mechanism(s) by which Hesa-A may improve clinical outcome of oral carcinoma by affecting oncogene erbb2 expression and suggest Hesa-A as an effective chemotherapeutic agent in treatment of HER+tumors.
 Keywords
Hesa-A;oral carcinoma;erbb2 expression;clinical outcome;rat model;invasion;
 Language
English
 Cited by
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Combination of nanotechnology with vascular targeting agents for effective cancer therapy, Journal of Cellular Physiology, 2017, 233, 4, 2982  crossref(new windwow)
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